DC Field | Value | Language |
---|---|---|
dc.contributor.author | Park H.-S. | ko |
dc.contributor.author | Kim M.-S. | ko |
dc.contributor.author | Chung, Jongkyeong | ko |
dc.contributor.author | Kang S.S. | ko |
dc.contributor.author | Huh S.-H. | ko |
dc.contributor.author | Park J. | ko |
dc.contributor.author | Choi E.-J. | ko |
dc.date.accessioned | 2013-03-03T13:54:32Z | - |
dc.date.available | 2013-03-03T13:54:32Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2002 | - |
dc.identifier.citation | JOURNAL OF BIOLOGICAL CHEMISTRY, v.277, no.4, pp.2573 - 2578 | - |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.uri | http://hdl.handle.net/10203/78957 | - |
dc.description.abstract | The protein serine-threonine kinase Akt mediates cell survival signaling initiated by various growth-promoting factors such as insulin. Here we report that SEK1 is a target of Akt in intact cells. Insulin inhibited the anisomycin-induced stimulation of both endogenous SEK1 and its substrate c-Jun N-terminal kinase (JNK), but not that of the upstream kinase MEKK1, in 293T cells. The inhibitory action of insulin on SEK1 or JNK1 activation was prevented by the phosphatidylinositol 3-kinase inhibitor LY294002. Expression of a constitutively active form of Akt also inhibited both SEK1 and JNK1 activation, but not that of MEKK1, in transfected 293T cells. Co-immunoprecipitation analysis revealed that endogenous Akt physically interacted with endogenous SEK1 in cells and that this interaction was promoted by insulin. In vitro and in vivo P-32 labeling indicated that Akt phosphorylated SEK1 on serine 78. The SEK1 mutant SEK1(S78A) was resistant to Akt-induced inhibition. Finally, activated Akt inhibited SEK1-mediated apoptosis, and this effect of Akt was prevented by overexpression of SEK(S78A). Taken together, these results suggest that Akt suppresses stress-activated signaling by targeting SEK1. | - |
dc.language | English | - |
dc.publisher | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC | - |
dc.subject | N-TERMINAL KINASE | - |
dc.subject | C-JUN | - |
dc.subject | TRANSCRIPTION FACTOR | - |
dc.subject | SIGNAL-TRANSDUCTION | - |
dc.subject | PHOSPHOINOSITIDE 3-KINASE | - |
dc.subject | CELL-SURVIVAL | - |
dc.subject | ACTIVATION | - |
dc.subject | JNK | - |
dc.subject | PATHWAY | - |
dc.subject | EXPRESSION | - |
dc.title | Akt (protein kinase B) negatively regulates SEK1 by means of protein phosphorylation | - |
dc.type | Article | - |
dc.identifier.wosid | 000173421500027 | - |
dc.identifier.scopusid | 2-s2.0-0037169526 | - |
dc.type.rims | ART | - |
dc.citation.volume | 277 | - |
dc.citation.issue | 4 | - |
dc.citation.beginningpage | 2573 | - |
dc.citation.endingpage | 2578 | - |
dc.citation.publicationname | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.identifier.doi | 10.1074/jbc.M110299200 | - |
dc.contributor.localauthor | Chung, Jongkyeong | - |
dc.contributor.nonIdAuthor | Park H.-S. | - |
dc.contributor.nonIdAuthor | Kim M.-S. | - |
dc.contributor.nonIdAuthor | Kang S.S. | - |
dc.contributor.nonIdAuthor | Huh S.-H. | - |
dc.contributor.nonIdAuthor | Park J. | - |
dc.contributor.nonIdAuthor | Choi E.-J. | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | N-TERMINAL KINASE | - |
dc.subject.keywordPlus | C-JUN | - |
dc.subject.keywordPlus | TRANSCRIPTION FACTOR | - |
dc.subject.keywordPlus | SIGNAL-TRANSDUCTION | - |
dc.subject.keywordPlus | PHOSPHOINOSITIDE 3-KINASE | - |
dc.subject.keywordPlus | CELL-SURVIVAL | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | JNK | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | EXPRESSION | - |
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